RAAS Physiology

The renin–angiotensin–aldosterone system (RAAS) is a pressure-preserving response. It becomes active when the kidney detects reduced effective circulating volume or reduced renal perfusion, then raises vascular tone and retains sodium and water. Juxtaglomerular cells in the afferent arteriole release renin in response to four principal signals: - reduced afferent arteriolar perfusion pressure; - reduced sodium and chloride delivery to the macula densa; - increased sympathetic activity through beta-1 receptors; and - humoral factors that promote renin release. Renin cleaves liver-produced angiotensinogen into angiotensin I. Angiotensin-converting enzyme converts angiotensin I into angiotensin II, the main active effector of the cascade. Angiotensin II constricts systemic arterioles, stimulates adrenal aldosterone secretion, increases proximal tubular sodium reabsorption, promotes antidiuretic hormone release, and stimulates thirst. Its renal vascular action is especially important. Angiotensin II constricts the efferent arteriole more than the afferent arteriole. This raises hydrostatic pressure within the glomerulus and helps preserve filtration when renal perfusion falls. The adaptation is useful during volume depletion, but it also means that some patients become dependent on angiotensin II to maintain their GFR. Aldosterone acts mainly on...